Ovarian cancer is the forth most common cause of death from cancer in women. Further, ovarian cancer is the leading cause of death among women with cancer of the female reproductive tract. As is the case with other common human carcinomas, a series of multiple genetic alterations are believed to be involved in the development of ovarian cancer. Some genetic abnormalities can alter the normal function of tumor suppressor gene products quantitatively and/or qualitatively and contribute to carcinogenesis. However, the genetic alterations involved in ovarian carcinoma remain largely unknown.
Despite the advances in imaging techniques and the availability of serum tumor markers (such as CA125), the majority of ovarian cancer patients are still diagnosed at an advanced stage of the disease--Stage III or IV. Although surgery and intensive chemotherapy have improved to a limited extent the response of ovarian cancer patients to treatment, recurrence and mortality among these patients remains a major problem. Clearly, the development of an early indicator of risk of ovarian cancer will be useful as a tool for early diagnosis and improving prognosis.
The p16 gene (or MST1 gene) has also been identified as a putative tumor suppressor gene. By binding to and inhibiting cyclin-dependent kinase (CDK4), which is activated by cyclin-D in the G1 phase of the cell cycle. It plays a critical role in regulation of normal cell growth. p16 could suppress cell division in a similar fashion to p21 by inhibiting the activity of cyclin-CDK complex. In addition, the p16 gene has already been shown on a high frequency of mutation in tumor cell lines however a much lower mutation frequency was detected in primary tumors.